Work overload alters expression of the Na+-K+-adenosinetriphosphatase (ATPase) multigene family in the myocardium. However, due to lack of an appropriate animal model, very little is known regarding regulation of the α3-isoform. We previously reported that adult ferret myocardium expresses the α1- and α3-isoforms of Na+-K+-ATPase. In the current study we examined the relative abundances of these isoforms in a recently developed ferret model of pressure-overload cardiac hypertrophy. Ferrets with abdominal aortic constriction (Coarc) developed significant left ventricular hypertrophy based on altered morphometric measurements and switching of the myosin heavy chain isoforms. Western and Northern blotting analyses showed that in hypertrophied left ventricles of Coarc ferrets the abundance of α1- protein increased (27%), whereas that of α1-mRNA remained unchanged. In nonhypertrophied right ventricles of Coarc ferrets abundance of α1-protein remained unchanged. Expression of the α3-isoform in left ventricles of Coarc ferrets remained unchanged at both protein and mRNA levels. By contrast, abundance of β1-mRNA increased significantly (31%), whereas β1- protein remained unchanged. Na+-K+-ATPase activity, estimated by K+- dependent nitrophenyl phosphatase activity, did not differ between left ventricular homogenates from Coarc and sham-operated ferrets. In conclusion, these studies indicate that in hypertrophied ferret heart Na+-K+-ATPase isoforms are differentially regulated at pretranslational, as well as at translational-posttranslational levels.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||3 35-3|
|State||Published - Jan 1 1994|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)